Related Experiment Video
Updated: Oct 5, 2025
10:33
Primed Mycobacterial Uveitis PMU as a Model for Post-Infectious Uveitis
Published on: December 17, 2021
2.8K
Late-onset Ocular Toxicity Presenting as Uveitis Caused by Crizotinib
Megumi Iseki1, Toshikatsu Kaburaki1, Makoto Aihara1
1Department of Ophthalmology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Neuro-Ophthalmology (Aeolus Press)
|January 31, 2022
Summary
Crizotinib, a lung cancer drug, can cause late-onset ocular toxicity, including optic disc edema and retinal changes. Symptoms resolved after switching to alectinib, suggesting drug-induced morphological alterations.
Area of Science:
- Ophthalmology
- Oncology
- Pharmacology
Background:
- Crizotinib is a targeted therapy for anaplastic lymphoma kinase-positive non-small cell lung cancer.
- Ocular side effects of crizotinib are known but late-onset presentations are less documented.
Observation:
- A 64-year-old female with lung cancer developed optic disc edema and retinal vascular leakage two years after starting crizotinib.
- Fluorescein angiography showed uveitis and leakage from optic disc, retinal veins, and capillaries.
Findings:
- The ocular findings persisted for over a year without vision loss.
- Discontinuation of crizotinib and initiation of alectinib led to immediate resolution of symptoms.
Implications:
- This case highlights the potential for late-onset ocular toxicity from crizotinib.
- It underscores the importance of monitoring for ocular changes in patients receiving crizotinib.
- The findings suggest crizotinib-induced morphological changes in the optic disc and retina.
Related Concept Videos
01:25Glaucoma: Overview
949
Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...
949
01:27Open Angle Glaucoma: Treatment
744
In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...
Drugs such as carbonic anhydrase inhibitors, α2- and...
744
01:22Photoreceptors and Visual Pathways
6.7K
At the molecular level, visual signals trigger transformations in photopigment molecules, resulting in changes in the photoreceptor cell's membrane potential. The photon's energy level is denoted by its wavelength, with each specific wavelength of visible light associated with a distinct color. The spectral range of visible light, classified as electromagnetic radiation, spans from 380 to 720 nm. Electromagnetic radiation wavelengths exceeding 720 nm fall under the infrared category,...
6.7K
01:28Angle Closure Glaucoma: Treatment
879
Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...
879